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  • 1
    Keywords: Forschungsbericht
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource (22 Seiten, 2,19 MB) , Illustrationen, Diagramme
    Series Statement: Bericht / Gemeinschaftsausschuss Verzinken 172
    Language: German , English
    Note: Förderkennzeichen AiF 19444 BG , Literaturverzeichnis: Seite 21 , Sprache der Kurzfassungen: Deutsch, Englisch
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  • 2
    Online Resource
    Online Resource
    Cambridge :Cambridge University Press,
    Keywords: Messier, Charles. ; Electronic books.
    Description / Table of Contents: This stunning atlas presents a complete account of each of the 110 Messier objects, with information on their history, astrophysical significance, and detailed observational descriptions. Illustrated with the finest color astrophotos, historical sketches and deep sky drawings - this is a must-have reference for observers of all ages and abilities!.
    Type of Medium: Online Resource
    Pages: 1 online resource (372 pages)
    Edition: 1st ed.
    ISBN: 9780511422638
    DDC: 523.112
    Language: English
    Note: Cover -- Half-title -- Title -- Copyright -- Table of contents -- Foreword -- Preface -- User guide -- The data files -- The texts -- The pictures -- Charles Messier -- 1730 to 1751: Childhood and adolescence -- 1751 to 1757: Assistant of the Naval Observatory -- 1759 to 1770: Comet discoveries and recognition -- 1770 to 1789: Changing private fortunes and observational successes -- 1789 to 1804: In the turmoil of the French Revolution -- The Observations -- Work on the catalog -- M 1 and M 2: Beginnings and motivation -- M 3 to M 40: Systematic search for nebulae -- M 41 to M 45: Completion of the first catalog -- M 46 to M 52: Further discoveries -- M 53 to M 70: Completion of the second catalog version -- M 71 to M 103: Méchain's discoveries and the final catalog version -- M 104 to M 109: After press -- The "missing" Messier objects -- M 47 -- M 48 -- M 91 -- M 102 -- The supplementary Messier objects -- M 104 -- M 105 -- M 106 -- M 107 -- M 108, M 109 -- The catalog -- Remarks on Messier's catalog -- 1 foot observed objects: M 3, M 5, M 13, M 33, M 41, M 92 -- 2 foot observed objects: M 2 -- 3 foot observed objects: M 8, M 10, M 11, M 25, M 26, M 30, M 34, M 35 -- 3.5 foot observed objects: M 14, M 17, M 18, M 19, M 22, M 23, M 26, M 27, M 28, M 29, M 30, M 32, M 36, M 37, M 39, M 49, M 51, M 81 -- 6 foot -- Statistics of the Messier objects -- The galactic nebulae -- The open clusters -- The planetary nebulae -- The globular clusters -- The galaxies -- The non-physical objects -- Visual observation of the Messier objects -- Photography of the Messier Objects -- M 1 The Crab Nebula -- M 2 -- M 3 -- M 4 -- M 5 -- M 6 The Butterfly Cluster -- M 7 -- M 8 with the Lagoon Nebula -- M 9 -- M 10 -- M 11 The Wild Duck Cluster -- M 12 -- M 13 The Great Hercules Cluster -- M 14 -- M 15 -- M 16 with the Eagle Nebula -- M 17 The Omega or Swan Nebula. , M 18 -- M 19 -- M 20 The Trifid Nebula -- M 21 -- M 22 -- M 23 -- M 24 The Small Sagittarius Star Cloud -- M 25 -- M 26 -- M 27 The Dumbbell Nebula -- M 28 -- M 29 -- M 30 -- M 31 The Andromeda Galaxy -- M 32 -- M 33 The Triangulum Galaxy -- M 34 -- M 35 -- M 36 -- M 37 -- M 38 -- M 39 -- M 40 -- M 41 -- M 42 The Great Orion Nebula -- M 43 -- M 44 The Beehive Cluster or Praesepe -- M 45 The Pleiades or Seven Sisters -- M 46 -- M 47 -- M 48 -- M 49 -- M 50 -- M 51 The Whirlpool Galaxy -- M 52 -- M 53 -- M 54 -- M 55 -- M 56 -- M 57 The Ring Nebula -- M 58 -- M 59 -- M 60 -- M 61 -- M 62 -- M 63 The Sunflower Galaxy -- M 64 The Black Eye Galaxy -- M 65 -- M 66 -- M 67 -- M 68 -- M 69 -- M 70 -- M 71 -- M 72 -- M 73 -- M 74 -- M 75 -- M 76 The Little Dumbbell Nebula -- M 77 -- M 78 -- M 79 -- M 80 -- M 81 -- M 82 -- M 83 -- M 84 -- M 85 -- M 86 -- M 87 -- M 88 -- M 89 -- M 90 -- M 91 -- M 92 -- M 93 -- M 94 -- M 95 -- M 96 -- M 97 The Owl Nebula -- M 98 -- M 99 -- M 100 -- M 101 The Pinwheel Galaxy -- M 102 -- M 103 -- M 104 The Sombrero Galaxy -- M 105 -- M 106 -- M 107 -- M 108 -- M 109 -- M 110 -- Glossary of technical terms -- Index of figures -- First chapters -- Main part -- Index of sources -- History -- Observation -- Distance data -- Individual objects.
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 161 (1998), S. 0 
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: In order to be able to study gene regulation in single, live Helicobacter pylori bacteria in vitro or in contact with host cells, we established the green fluorescent protein gene gfp from Aequorea victoria as a reporter gene for use with Helicobacter species. We describe here the construction of genomic transcriptional fusions of the promoterless gfp gene with the flaA and flaB promoters of H. pylori. We have also constructed a Mini-Tn3-km-gfp transposon to be used for shuttle transposon mutagenesis in H. pylori and H. mustelae. A marker strain with wild-type phenotype, carrying multiple plasmid-borne copies of gfp under the control of the H. pylori flaB promoter, was constructed for studies of bacterial distribution and transmission in animal models.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Helicobacter pylori possesses a gene (HP0326/JHP309) homologous to neuA of other bacteria, encoding a cytidyl monophosphate-N-acetylneuraminic acid synthetase-homologous enzyme in its N-terminal portion. We analysed the function of this gene, which is controlled by a flagellar class 2 σ54 promoter, in flagellar biosynthesis. HP0326/JHP309 actually represents a bicistronic operon consisting of a neuA and a flmD-like putative glycosyl transferase gene. An isogenic flmD mutant synthesized basal bodies but no filaments, was non-motile, and expressed severely reduced amounts of a FlaA flagellin of reduced molecular mass. FlaA flagellin was found to be glycosylated in its exported form within the flagellar filament, but not inside the cytoplasm. Glycosylated FlaA was not detectable in the flmD mutant. Together with other genes in the H. pylori genome, a proposed function of the neuA/flmD gene products could be to provide a pathway for glycosylation of flagellin and other extracytoplasmic molecules during type III secretion.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Molecular microbiology 20 (1996), S. 0 
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 6
    Publication Date: 2014-06-28
    Description: Analyzing a patient with progressive and severe cardiac conduction disorder combined with idiopathic ventricular fibrillation (IVF), we identified a splice site mutation in the sodium channel gene SCN5A . Due to the severe phenotype, we performed whole-exome sequencing (WES) and identified an additional mutation in the KCNK17 gene encoding the K 2P potassium channel TASK-4. The heterozygous change (c.262G〉A) resulted in the p.Gly88Arg mutation in the first extracellular pore loop. Mutant TASK-4 channels generated threefold increased currents, while surface expression was unchanged, indicating enhanced conductivity. When co-expressed with wild-type channels, the gain-of-function by G88R was conferred in a dominant-active manner. We demonstrate that KCNK17 is strongly expressed in human Purkinje cells and that overexpression of G88R leads to a hyperpolarization and strong slowing of the upstroke velocity of spontaneously beating HL-1 cells. Thus, we propose that a gain-of-function by TASK-4 in the conduction system might aggravate slowed conductivity by the loss of sodium channel function. Moreover, WES supports a second hit-hypothesis in severe arrhythmia cases and identified KCNK17 as a novel arrhythmia gene. A novel exonic mutation in the K 2P potassium channel TASK-4 is found in a patient with severe PCCD, resulting in a gain-of-function that could explain the severe progressive conduction disorder compared to isolated loss-of-function mutations in SCN5A channels.
    Print ISSN: 1757-4676
    Electronic ISSN: 1757-4684
    Topics: Medicine
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